Ebook Skeletal radiology the bare bones (3rd edition): Part 2

(BQ) Part 2 book Skeletal radiology the bare bones presents the following contents: Approach to joint disease, inflammatory arthritis, noninflammatory joint disease, developmental and congenital conditions, metabolic and systemic conditions, infection and marrow disease, postsurgical imaging.

Joint Disease

Distribution of DiseaseLaboratory Findings

his chapter describes a pragmatic approach to the radiology

of joint disease, based on anatomy, pathophysiology, and radiographic analysis This approach draws heavily on the work of Forrester, Brower, and Resnick (Table 11.1) Detailed

discussions of specifi c clinical forms of arthritis are presented in

Chapters 12 and 13

GENERAL PRINCIPLES

Radiographs mirror the pathologic processes that affect the joints

and the functional adaptations that may follow In general, the

radiologic diagnosis of arthritis can be highly specifi c and reliable

when classic changes are present in the expected distributions but

much less specifi c in the early stages before the disease process has

fully evolved Regardless of the approach, however, several

frustra-tions are unavoidable: A specifi c radiologic diagnosis is not always

possible; many types of joint disease overlap in their radiologic

and clinical features; two or more diseases may coexist in the same

patient; and, fi nally, clinical disease may precede radiologic

abnor-malities and vice versa, sometimes by years

Diseases that affect joints do so by three broad

pathophysi-ologic mechanisms, each with a distinctive radiographic

appear-ance: degeneration, infl ammation, and metabolic deposition

For practical purposes, one mechanism is usually predominant

Degeneration of a joint refers to mechanical damage and

repara-tive adaptations; in essence, the joint is worn away Infl ammation

of a joint may be acute, chronic, or both; the joint is dissolved by the infl ammatory process Metabolic deposition refers to the infi l-tration of a joint by aberrant metabolic products Each of these mechanisms affects joints in radiographically distinctive ways (Table 11.2)

SYNOVIAL JOINTS

Most articulations of the appendicular skeleton are synovial joints

In the axial skeleton, the facet joints of the spine, the atlantoaxial (C1–2) joint, the uncovertebral joints of the cervical spine, and the lower two thirds of the sacroiliac joints are synovial

Soft Tissues

Synovial joints have a joint cavity and are enclosed by a joint capsule consisting of an inner synovial layer (the synovium), a middle sub-synovium, and an outer fi brous layer (Fig 11.1) The synovium is a cellular secretory mucosa that produces synovial fl uid Synovial fl uid

is viscous because of a high concentration of hyaluronic acid Joint capsules have an active blood supply with a large capillary surface area The synovium has a mesenchymal rather than epithelial ori-gin; therefore, no basement membrane or other structural barrier is present between the synovial fl uid and the capillary bed The change from synovium to fi brous capsule is gradual; there are no distinct

T

TAB LE 11.1 Approach to Radiographic Analysis

of Arthritic Changes in the Hand

Source : Data from Brower AC Arthritis in Black and White 2nd Ed

Philadelphia, PA: WB Saunders; 1997 and Forrester DM, Brown JC The

Radiology of Joint Disease 3rd Ed Philadelphia, PA: WB Saunders; 1987

TAB LE 11.2 Characteristic Radiographic Signs

of Arthritis

Pathophysiology Characteristic Radiographic SignsInfl ammation Acute erosions

OsteoporosisSoft-tissue swellingUniform loss of articular spaceDegeneration Osteophytes

Subchondral sclerosisUneven loss of articular spaceChondrocalcinosis

Metabolic deposition Lumpy-bumpy soft-tissue swelling

Chronic bony erosions with overhanging edges

boundaries between the layers Joint capsules are densely innervated

Tendon sheaths invest tendons and reduce friction during motion

Bursae are located where complete freedom of motion between

structures is necessary, for example, where a tendon passes directly

over the periosteum Because tendon sheaths and bursae are synovial

structures, diseases that affect synovial joints may also involve them

Soft-tissue swelling at a joint may refl ect capsular

disten-tion from effusion, synovial hypertrophy, soft-tissue edema, or

a mass Symmetric, fusiform swelling suggests an infl ammatory

process with effusion, synovial edema, synovial hypertrophy, or

some combination thereof (Fig 11.2) Infl ammatory distention

of a tendon sheath may also produce soft-tissue swelling, but the

swelling extends beyond the joint In a digit, this kind of swelling

FIGURE 11.2 Fusiform soft-tissue swelling at the PIP joint

(rheuma-toid arthritis)

produces an appearance that has been likened to a sausage (sausage digit) Generalized soft-tissue swelling may be caused by subcuta-neous edema or hyperemia and suggests infl ammation (Fig 11.3)

Lumpy-bumpy swelling that is not symmetric or centered near a joint suggests masses and may be caused by metabolic deposition disease with masslike deposits of metabolic products in the periar-ticular soft tissues (Fig 11.4) Soft-tissue prominences at joints that

FIGURE 11.3 “Sausage digit” soft-tissue swelling (psoriatic arthritis).

FIGURE 11.4 Lumpy-bumpy soft-tissue swelling (tophaceous gout).

FIGURE 11.1 Anatomy of a synovial joint.

are found on physical examination may actually result from bony or

cartilaginous enlargements; the overlying soft tissues may be

nor-mal Heberden and Bouchard nodes are swellings of this kind at the

distal interphalangeal (DIP) and proximal interphalangeal (PIP)

joints of the hand, respectively, and are characteristic of a

degen-erative process Calcifi cation in the soft tissues may affect cartilage,

skin, muscles, tendons, or other connective tissues and is associated

with connective tissue diseases Soft-tissue atrophy or loss is present

in various conditions

Cartilage

The ends of the articulating bones, that is, the joint surfaces, are

covered with hyaline articular cartilage Hyaline cartilage is

com-posed of a collagen fi bril framework and a ground substance One

set of densely packed collagen fi brils is oriented parallel to the

articular surface, forming an armor-plate layer with tiny surface

pores that allow the passage of water and small electrolytes A

sec-ond, less densely packed set of collagen fi brils is oriented in arcades,

FIGURE 11.5 Structure of articular cartilage.

FIGURE 11.6 Asymmetric joint space narrowing, osteophytes, and

subchondral sclerosis (osteoarthritis)

FIGURE 11.7 Severe PIP joint subchondral bone erosions (psoriatic

arthritis)

linking the armor-plate layer to the subchondral bone (Fig 11.5)

The ground substance is a gel that consists of water and large proteoglycan aggregate macromolecules that are loosely fi xed to the collagen framework The proteoglycan macromolecules are too large to pass through the pores of the armor-plate layer The physi-cal and chemical properties of these macromolecules allow them

to attract and bind water, providing suffi cient swelling pressure beneath the armor-plate layer to “infl ate” the articular cartilage, even during weight bearing During motion, a thin layer of water

is expressed through the small surface pores, providing a less surface for a lifetime of mobility Articular cartilage has a load-dampening ability that spreads transmitted loads over a greater area

friction-of the subchondral bone Under rapid, transient loading, articular cartilage has elastic properties Under a steady load, it creeps and deforms like a sponge The portion of cartilage that is adjacent to the subchondral bone is calcifi ed Interdigitations between the cal-cifi ed cartilage and the subchondral bone provide a strong mechan-ical coupling Chondrocytes are the cells whose metabolic activity maintains the specialized structures of articular cartilage Less than 1% of articular cartilage volume is composed of cells Because car-tilage is avascular and alymphatic, chondrocytes derive their nutri-ents by diffusion from the synovial fl uid Articular cartilage has only a limited ability to repair itself Deep injuries may repair with cartilage that is densely fi brous

Cartilage abnormalities are inferred from the radiolucent gap between articulating bones, the articular space, or the joint space

The articular cartilage fi lls this space A potential space exists where the articulating surfaces meet Loss of articular cartilage causes the joint space to narrow Cartilage loss within a joint can

be diffuse and concentric—indicating an infl ammatory process (with enzymatic dissolution of cartilage)—or focal and uneven, indicating a mechanical one (Fig 11.6) If there is complete

FIGURE 11.8 Bony ankylosis (psoriatic arthritis).

FIGURE 11.9 Chondrocalcinosis of the menisci (arrowheads).

FIGURE 11.10 Chondrocalcinosis of the articular cartilage (arrow).

cartilage loss, the ends of the bones may become eroded, making

the joint space appear wider The ends of the bone may form a

pseudoarthrosis (Fig 11.7), or fi brous or bony ankylosis (fusion)

of the joint may occur (Fig 11.8) Widening of the articular space

may indicate abnormal cartilage proliferation or intra-articular

fl uid Weight-bearing views may be necessary to assess accurately

the degree of cartilage loss at the knee Asymmetric cartilage loss may result in changes in radiographic joint space narrowing with changes in position

Calcifi cation of cartilage is called chondrocalcinosis

Chondro-calcinosis may involve fi brocartilage structures such as the menisci

of the knee (Fig 11.9) or the triangular fi brocartilage complex of the wrist Articular cartilage also may calcify (Fig 11.10)

Bone

Bone changes in arthritis include bone loss and bone tion Osteoporosis is the loss of bone through osteoclast action and may be generalized or regional, acute or chronic Osteoporosis refl ects hyperemia from synovial infl ammation or from the disuse

prolifera-of a body part Acute osteoporosis is recognized by the resorption

of bone from subchondral trabeculae, a location where blood fl ow and metabolic activity are the greatest The process of osteoporosis affects the trabecular bone and the cortex However, because the surface area subject to osteoclastic resorption is greater in the tra-becular bone, the acute process is more evident there If the process continues, tunneling may become evident in the cortex and can be recognized as being porotic and thin In noninfl ammatory articular disease, the normal mineralization of bone is maintained Arthritic conditions are commonly treated with corticosteroids, which may cause osteoporosis

Bone erosions represent focal losses of bone from the cortical surface Erosions with loss of the cortex indicate an acute, aggres-sive process In rheumatoid arthritis, for example, the cortical bone

is eroded by the action of enzymes produced by infl amed ovial tissues (pannus) These enzymes literally dissolve the bone and produce acute erosions without cortex (Fig 11.11) Erosions with cortex indicate a nonaggressive, chronic process in which the bone remodels along the border of the erosion The chronic ero-sions seen in metabolic deposition disease are caused by abnormal masses of metabolic products causing the adjacent bone to remodel because of mechanical pressure The bone may attempt to encircle the deposit; such an incomplete attempt leaves an overhanging edge

syn-FIGURE 11.12 Chronic erosion and overhanging edges (tophaceous

gout)

FIGURE 11.13 Subchondral cyst formation (rheumatoid arthritis)

(arrow).

FIGURE 11.14 Periostitis (psoriatic arthritis) (arrows).

FIGURE 11.11 Acute marginal erosions (arrows), diffuse joint space

narrowing, and osteoporosis (rheumatoid arthritis)

(Fig 11.12) Other masslike processes in the joint may also cause

chronic erosions of the bone The characteristic initial site of

ero-sions in arthritis is at the margin of the articular cartilage where

a gap between the cartilage and the attachment of the synovium

leaves a “bare area” of bone contained within the joint capsule

Once cartilage has been destroyed, erosions may extend over the entire articular surface

Subchondral cysts, also called geodes, occur when cracks or fi

s-sures in the articular surface allow the intrusion of synovial fl uid into the subchondral cancellous bone or when necrosis of the sub-chondral bone is followed by collapse (Fig 11.13) Subchondral cysts may also result from erosions of the articular surface by infl amed synovial tissues Subchondral cysts are seen in virtually all types of arthritis and have no particular differential diagnostic signifi cance

Proliferative new bone may represent attempts at cyst healing

Proliferative bone formation at arthritic synovial joints occurs

in four ways Periostitis is the periosteal apposition of a new bone to

the cortical surface (Fig 11.14) Sclerosis, also called eburnation, is

Abnormalities of alignment resulting from articular disease are common at the wrist, knee, and foot Alignment deformities

of the wrist may follow or precede actual articular changes on radiographs; these misalignments may have great clinical signifi -cance because normal wrist function is a prerequisite for normal hand function The ligamentous instability patterns that may fol-low traumatic disruption of the carpal ligaments (see Chapter 2) may also result from the arthritic involvement of the carpal liga-ments Selective involvement of the medial or lateral tibiofemoral compartment of the knee with asymmetric thinning of cartilage may lead to varus or valgus deformity In the foot, various dig-ital deformities similar to those occurring in the hand may be found

INTERVERTEBRAL DISK JOINTS

Intervertebral disk joints are present along the anterior portion

of the spine An intervertebral disk joint comprises cartilaginous end plates covering the articulating surfaces of adjacent vertebral bodies, a central nucleus pulposus, and a circumferential annulus

fi brosus (Fig 11.16) In the child, the nucleus pulposus has a nous character; in the adult, the nucleus pulposus has converted

gelati-to fi brocartilage The annulus fi brosus contains an outer zone of collagenous fi bers and an inner zone of fi brocartilage The annulus

fi brosus is anchored to the cartilaginous end plates, the vertebral rim, and the periosteum of the vertebral body The anterior longi-tudinal ligament is applied to the anterior aspect of the vertebral column with fi rm attachments to the periosteum near the corners

of the vertebral bodies A posterior longitudinal ligament is applied

to the posterior aspect of the vertebral bodies The same structure and physiology are found at the symphysis pubis

In the anterior column of the spine, one may evaluate ment, intervertebral spaces, and bone changes Soft-tissue changes

align-in the axial skeleton are diffi cult to recognize Abnormalities of alignment include intervertebral subluxation, exaggerated kypho-sis or lordosis, kyphosis or lordosis at inappropriate levels, and scoliosis Films of the patient in fl exion, extension, or lateral bend-ing may be required to demonstrate abnormal mobility or loss of mobility

The intervertebral disk spaces should be proportionate to the width of the vertebral body They are relatively small in the cervical

a new bone apposed to the trabeculae of the existing bone, usually

in a subchondral location (immediately beneath the articular

car-tilage) but sometimes on the surface after the cartilage is gone

Osteophytes occur in the presence of cartilage loss and represent

new excrescences of cartilage and bone that enlarge the articular

surface at its margins Bony proliferation may also occur at the

attachment of joint capsules (discussed in the “Entheses”)

Alignment

Alignment becomes abnormal when joint capsules or ligaments are

torn or lax, the normally balanced tension across joints becomes

unbalanced, or articular surfaces lose their normal size or shape

The result is deformity, subluxation, dislocation, and loss of

tion Continued use of a damaged, malaligned joint leads to

func-tional adaptation and secondary anatomic changes; ultimately, it

may become diffi cult to distinguish these functional adaptations

from the primary arthritic process Loss of function and pain are

the major causes of morbidity in arthritis

Alignment deformities in the hand may lead to a functional

dis-ability of great clinical signifi cance Deformities of the hand result

from loss of the balanced muscular tension and ligamentous

restric-tion that maintain its normal alignment Common deformities of

the digit include the swan neck deformity (PIP hyperextension with

DIP fl exion) (Fig 11.15A), the boutonniere deformity (PIP fl exion

with DIP hyperextension) (Fig 11.15B), the mallet fi nger (isolated

DIP fl exion), and the hitchhiker thumb or Z-shaped collapse of the

thumb (metacarpophalangeal [MCP] joint fl exion,

interphalan-geal [IP] joint hyperextension) Subluxations and dislocations of

individual joints may be seen, or the entire hand may collapse into

a zigzag deformity (radial deviation of wrist with ulnar deviation

of the MCP joints) These deformities refl ect loss of normal

func-tional anatomy from any underlying cause, one of which may be

arthritis

FIGURE 11.15 Rheumatoid arthritis A: Swan neck deformity

B: Boutonniere deformity FIGURE 11.16 Anatomy of an intervertebral disk joint.

FIGURE 11.17 Syndesmophytes (arrow) formed by the ossifi cation of

the outer layers of the annulus fi brosus (ankylosing spondylitis)

region but gradually become thicker in the thoracic and lumbar

regions Narrowing is characteristic of degenerative disk disease,

and calcifi cation or gas in the disk space is pathognomonic

The morphology of bony outgrowths along the spine, called

vertebral phytes, may be of great diagnostic value (Table 11.3)

Ossi-fi cation in the periphery of the annulus Ossi-fi brosus may lead to a shell

of bone that bridges the intervertebral space (Fig 11.17) These are

called bridging syndesmophytes and are characteristic of ankylosing

spondylitis Ossifi cation of the anterior longitudinal ligament along

multiple contiguous levels is characteristic of diffuse idiopathic

skel-etal hyperostosis (DISH) This ossifi cation is often exuberant and

adjacent to, but separate from, the vertebral body (Fig 11.18)

Osteo-phytes are horizontal extensions of the vertebral end plates that have

a triangular confi guration (Fig 11.19) If suffi ciently large

osteo-phytes are present at adjacent end plates, they may form an

extra-articular bridge across the intervertebral space Small osteophytes are

associated with degenerative conditions Large, focal, paravertebral

Vertebral Phytes: Associations With Specifi c Diseases

Type of Phyte Associated Condition

Syndesmophytes Ankylosing spondylitis

Diffuse, fl owing paravertebral

ossifi cation

DISHOsteophytes Degenerative disk

disease, spondylosis deformans

Focal paravertebral ossifi cation Psoriatic arthritis

(common), Reiter syndrome (uncommon)

TAB LE 11.3

soft-tissue ossifi cations are seen in psoriatic arthritis and Reiter syndrome These bony excrescences often become coalescent and contiguous with the vertebral bodies, resulting in extra- articular

FIGURE 11.18 Diffuse, fl owing ossifi cation (arrows) of the paravertebral soft tissues (DISH) A: Sagittal CT

reformation shows the ossifi cation (arrows) extending over multiple contiguous levels B: Axial CT shows the

ossifi cation (arrow) is asymmetric.

FIGURE 11.19 Triangular osteophytes (arrows) of spondylosis

defor-mans with degenerative disk changes The disk space is narrowed and

the subchondral bone is sclerotic

bridges along the lateral aspect of the spinal column (Fig 11.20)

Typically, they occur along the lateral aspects of the vertebral bodies

and do not involve multiple, contiguous levels on the same side

ENTHESES

An enthesis is the site of bony insertion of a tendon, ligament, or

articular capsule Tendons, ligaments, and articular capsules are

FIGURE 11.20 Ossifi cation in the paraspinal soft tissues leading to a bridging phyte (arrows) (reactive arthritis)

A: AP radiograph B: Axial CT and coronal reformation.

strong bands or sheets of collagen fi bers in a parallel ment Near the attachment to bone, chondrocytes are interspersed between the collagen fi bers The collagen fi bers in the bands or sheets become more compact, then cartilaginous, and fi nally cal-cifi ed as they enter the bone (Fig 11.21) The interdigitation of calcifi ed cartilage and bone provides a strong attachment Entheses have an active blood supply and a prominent innervation Enthesop-athy is a disease at an enthesis Enthesophytes and the calcifi cation and ossifi cation of an enthesis are the principal radiographic signs

arrange-of enthesopathy (Fig 11.22) Ossifi cation usually proceeds from the bony attachment into the substance of the inserting structure

MRI may directly demonstrate infl ammatory and degenerative changes of tendons and ligaments much earlier than radiographs

Normal tendons and ligaments have low signal on both T1- and T2-weighted MRI Fluid, edema, and myxoid change within ten-dons or ligaments are identifi able as regions of high signal

DISTRIBUTION OF DISEASE

There are two clinical situations: monarticular arthritis (one joint affected) and polyarticular arthritis (many joints affected) The differential diagnosis of monarticular arthritis is rather limited (Table 11.4) Each type of polyarticular arthritis has a predilection for specifi c sites in the skeleton and can often be recognized simply from the distribution of involvement (Table 11.5) The explanation for the highly specifi c distributions of disease is unknown There are some joints in the hand and foot where involvement can be vir-tually diagnostic of specifi c types of degenerative or infl ammatory polyarticular arthritis (Table 11.6)

In the hand, degenerative involvement of multiple DIP joints suggests osteoarthritis, whereas infl ammatory involvement sug-gests psoriatic arthritis Degenerative involvement of multiple MCP joints suggests pyrophosphate arthropathy, whereas infl ammatory involvement of the MCP joints suggests rheumatoid arthritis

FIGURE 11.22 Enthesophyte (arrow) at the insertion of the triceps

tendon

Degenerative involvement of the fi rst carpometacarpal (CMC)

joint suggests osteoarthritis Infl ammatory involvement of multiple

intercarpal joints suggests rheumatoid arthritis, psoriatic arthritis,

or gouty arthritis Degenerative involvement of the radiocarpal

joint suggests pyrophosphate arthropathy In the foot, degenerative

involvement of the fi rst metatarsophalangeal (MTP) joint suggests

osteoarthritis Infl ammatory involvement of the combination of

multiple MTP and IP joints suggests psoriatic arthritis or Reiter

syndrome, whereas infl ammatory involvement of multiple MTP

joints without IP joint involvement suggests ankylosing

spondyli-tis or rheumatoid arthrispondyli-tis Degenerative involvement of the fi rst

tarsometatarsal (TMT) joint suggests osteoarthritis Infl tory involvement of multiple intertarsal joints suggests rheumatoid arthritis Degenerative involvement of the talonavicular joint sug-gests pyrophosphate arthropathy

LABORATORY FINDINGS

Abnormal fi ndings on laboratory examinations are integral to the diagnosis of joint diseases They are most valuable when correlated with radiographs and other clinical information Material for labo-ratory analysis is usually obtained from blood or the joint Synovial

fl uid can be obtained by needle aspiration Samples of the synovial membrane, articular cartilage, or periarticular soft tissues are usu-ally obtained by biopsy

Rheumatoid factor (RF) is a group of nonspecifi c bodies found not only in the serum of patients with rheumatoid arthritis but also in that of patients with other acute and chronic infl ammatory diseases These include viral infections such as AIDS, mononucleosis, and infl uenza; chronic bacterial infections such as tuberculosis and subacute bacterial endocarditis; parasitic infections; neoplasms after chemotherapy or radiotherapy; and various hyperglobulinemic states The sensitivity and specifi city

autoanti-of detecting RF vary with the particular method autoanti-of measurement

The most common method is the latex fi xation test, in which the patient’s serum is challenged with latex particles coated with heat-treated human immunoglobulin G A positive result—that

is, agglutination of the latex particles because of the presence of RF—makes the patient seropositive or RF positive A negative result also has a clinical importance because it is one factor that distinguishes rheumatoid arthritis from the clinically overlapping group of seronegative spondyloarthropathies The strength of a positive result has therapeutic and prognostic signifi cance Never-theless, only 80% of patients with classic rheumatoid arthritis are

RF positive, as are 30% of patients with nonrheumatic diseases, 25% of patients with other rheumatic diseases, and 5% of the nor-mal population

ANA are a heterogeneous population of serum antibodies that react to various human nuclear components, including DNA They are detected by an immunofl uorescence screening test A positive ANA test is an empiric marker for connective tissue disease The test is positive in nearly all patients with systemic lupus erythe-matosus, scleroderma, and mixed connective tissue disease and in approximately 80% of patients with polymyositis/dermatomyositis

The actual pathogenetic signifi cance is unclear Changes in serum ANA levels may parallel the clinical course and be used to follow the activity of the disease

Common Causes of Monarticular Arthritis

Crystal relatedHemophiliac arthropathyRheumatoid (including juvenile chronic arthritis)Infectious

Synovial lesions (chondromatosis, PVNS)Traumatic

TAB LE 11.4

FIGURE 11.21 Anatomy of an enthesis.

HLA antigens represent a polymorphic group of inherited

antigens found on the surface membranes of cells; HLA antigens

have an uncertain biologic role The genes for HLA antigens are

located on the sixth chromosome in the major histocompatibility

complex Although it is well established that certain specifi c HLA

antigens are associated with certain rheumatic diseases, the precise

relationship of these genetic markers to disease is unclear HLA

antigens may infl uence not only the likelihood of a disease but also

the age of onset, severity, and individual clinical features There are three major associations of HLA antigens with rheumatic diseases:

(a) HLA-B27 with ankylosing spondylitis, Reiter syndrome, psoriatic arthritis, and enteropathic arthritis; (b) HLA-Cw6 with psoriasis and psoriatic arthritis; and (c) HLA-DR4 with rheumatoid arthritis The strongest association is between HLA-B27 and ankylosing spondyli-tis The prevalence of this antigen in patients with ankylosing spon-dylitis is 90%, compared with 9% in the general white population

Distribution of Polyarticular Arthritis

Arthritis Symmetry Predominant Sites of Involvement

Rheumatoid arthritis Symmetric Hand (PIPs, MCPs), wrist (pancompartmental), elbow,

shoulder, hip, knee, foot (multiple intertarsal, MTPs), and cervical spine

Ankylosing spondylitis Symmetric SI joint, ascending to lumbar, thoracic, and cervical spine,

hip, and foot (MTPs)Reiter syndrome Asymmetric SI joint, foot (MTPs, IPs, calcaneus), and lumbar spine

Psoriatic arthritis Asymmetric Hand (often entire rays), wrist, foot (MTPs, IPs,

calca-neus), lumbar spine, and SI jointPrimary osteoarthritis Asymmetric Hand (DIPs, PIPs, fi rst CMC), knee (especially medial

compartment), hip (superolateral or medial), and foot (fi rst MTP, fi rst TMT)

CPPD deposition disease Asymmetric Wrist (radiocarpal), shoulder (glenohumeral), knee

(especially patellofemoral), elbow, ankle, and foot (talonavicular)

Gout Asymmetric Hand (random joints), elbow, knee, and foot (fi rst MTP

and random joints)

TAB LE 11.5

Polyarticular Arthritis: Sites that Suggest Specifi c Diseases When Involved by Degenerative

or Infl ammatory Changes

Involved Site(s) Type of Joint Changes Degenerative Infl ammatory

Hand and Wrist

Multiple DIP joints Osteoarthritis Psoriatic arthritis

Multiple MCP joints CPPD deposition disease Rheumatoid arthritis

First CMC joint Osteoarthritis

Multiple intercarpal joints Rheumatoid arthritis

Psoriatic arthritisGouty arthritis Radiocarpal joint CPPD deposition disease

Foot

First MTP joint Osteoarthritis

Multiple MTP and IP joints Psoriatic arthritis

Reiter syndrome

Rheumatoid arthritis First TMT joint Osteoarthritis

Multiple intertarsal joints Rheumatoid arthritis

Talonavicular joint CPPD deposition disease

TAB LE 11.6

Koopman WJ, Boulware DW, Heudebert G Clinical Primer of

Rheumatol-ogy Philadelphia, PA: Lippincott Williams & Wilkins; 2003.

Koopman WJ, Moreland LW, eds Arthritis and Allied Conditions: A

Text-book of Rheumatology 15th Ed Philadelphia, PA: Lippincott Williams &

Resnick D, Niwayama G Entheses and enthesopathy Anatomical,

patho-logical, and radiological correlation Radiology 1983;146:1–9.

Salvarani C, Cantini F, Olivieri I, et al Magnetic resonance imaging and

polymyalgia rheumatica J Rheumatol 2001;28:918–919.

SOURCES AND READINGS

Brower AC Arthritis in Black and White 2nd Ed Philadelphia, PA: WB

Saunders; 1997

eMedicine http://emedicine.medscape.com

Firestein GS, Budd RC, Harris ED Jr, et al Kelley’s Textbook of Rheumatology

8th Ed Philadelphia, PA: Saunders; 2008

Forrester DM, Brown JC The Radiology of Joint Disease 3rd Ed Philadelphia,

PA: WB Saunders; 1987

Frediani B, Falsetti P, Storri L, et al Quadricepital tendon enthesitis in

psoriatic arthritis and rheumatoid arthritis: Ultrasound examinations

and clinical correlations J Rheumatol 2001;28:2566–2568.

Griffi n LY Essentials of Musculoskeletal Care 3rd Ed Rosemont, IL: American

Academy of Orthopedics; 2005

Groshar D, Rozenbaum M, Rosner I Enthesopathies, infl ammatory

spondy-loarthropathies and bone scintigraphy J Nucl Med 1997;38:2003–2005.

12 Infl ammatory Arthritis

Rheumatoid Arthritis

Pathologic-Radiologic Features

Hand and Wrist

Other Peripheral Joints

Spine

Extra-Articular Manifestations

Connective Tissue Disease

Systemic Lupus Erythematosus

Scleroderma

Dermatomyositis and PolymyositisOverlap SyndromesSpondyloarthropathyAnkylosing SpondylitisReactive ArthritisPsoriatic ArthritisEnteropathic SpondyloarthropathyDifferential Diagnosis

Juvenile Idiopathic ArthritisSeptic Arthritis

MiscellaneousGranulomatous SynovitisViral Synovitis

Lyme Disease

T his chapter covers those clinical forms of arthritis and con-nective tissue disease that present on radiographs with a

preponderance of infl ammatory changes

RHEUMATOID ARTHRITIS

Rheumatoid arthritis is a systemic autoimmune disease manifested

in the musculoskeletal system by infl ammatory polyarthritis of the

small synovial joints The pathogenesis is not understood, and no

causative agent has been proved Genetic factors affect

susceptibil-ity to and expression of the disease Rheumatoid arthritis is usually

distinguished from other arthritides by the presence of rheumatoid

factor (RF) in the serum (see Chapter 11) Rheumatoid arthritis has

a prevalence of 1% in the general population, with women affected

more often than men by a 3:1 ratio High RF titers often correlate

with more severe disease The typical age range of presentation is

25 to 55 years In 70% of cases, the onset is insidious and occurs

over weeks to months; in 20%, the onset occurs over days to weeks;

and in 10%, the onset is acute and occurs over hours to days The

acute onset mimics the onset of septic arthritis The clinical course

of rheumatoid arthritis is progressive in 70% of cases, leading to

disabling, destructive disease The clinical progression may be rapid

or slow In 20%, the disease is intermittent with remissions

gener-ally lasting longer than exacerbations, and in 10%, remissions last

several years The clinical diagnosis is based on criteria that include

morning stiffness, symmetric swelling of the proximal

interphalan-geal (PIP) joint, metacarpophalaninterphalan-geal (MCP) or wrist joints,

rheu-matoid nodules, serum RF, and specifi c radiographic fi ndings

Pathologic-Radiologic Features

The underlying pathologic change in rheumatoid arthritis is chronic

synovial infl ammation with hyperemia, edema, and production of

excess fl uid Chronicity leads to hypertrophy and fi brosis

Hyper-trophic, chronically infl amed synovium is called pannus Pannus

dissolves the cartilage and bone by the actions of enzymes along

its advancing margin Commonly seen early radiographic fi ndings

include fusiform periarticular soft-tissue swelling—corresponding

to synovial hypertrophy and joint effusion—and acute erosions at the margins of the joint Articular cartilage may also be dissolved by enzymes released into the joint space, causing uniform narrowing

of the joint space on radiographs Synovial hyperemia causes articular osteoporosis There is a characteristic lack of reactive bone formation Common late radiologic fi ndings include chronic gen-eralized osteoporosis, progression of marginal erosions to severe erosions involving subchondral bone, synovial cyst formation, sub-luxations and abnormalities of alignment, and secondary osteoar-thritis Not all fi ndings are present at any one time in individual patients; observation of combinations of these fi ndings should lead

juxta-to the correct diagnosis The distinctive radiographic pattern of chronic osteoporosis, marginal erosions, and little if any reactive bone formation is the hallmark of rheumatoid arthritis Although the appendicular skeleton tends to be extensively involved, the axial skeleton is usually spared except for the upper cervical spine

Bilaterally symmetric clinical involvement is usual, but the severity

of radiologic involvement is not necessarily symmetric, especially when radiographs are obtained early in the clinical course Second-ary degenerative changes may occur if the infl ammatory process remits for several years Both rheumatoid arthritis and primary osteoarthritis are common conditions; patients with both diseases may have confusing radiographic fi ndings

Sonography and MRI are more sensitive than radiography in detecting synovitis, the primary abnormality in rheumatoid arthri-tis Subchondral bone marrow edema may occur with synovitis, and both are precursors of bone erosions Erosions will not occur

in the absence of synovitis MRI criteria for diagnosing rheumatoid arthritis include periarticular contrast enhancement of the wrist

or the MCP or PIP joints in both hands, marrow edema, erosions, joint effusion, synovial sheath effusion, and cartilage irregularity and thinning Gadolinium helps distinguish nonenhancing joint

fl uid from enhancing synovial proliferation and pannus ful treatment of early rheumatoid arthritis with disease-modifying antirheumatic drugs that suppress synovitis may be evident on MRI

Success-as the reversion of synovitis and marrow edema to normal MRI is

FIGURE 12.1 Rheumatoid hand A boutonniere deformity is

pres-ent at the middle fi nger Erosions are prespres-ent at the PIP joint of the

middle fi nger (short arrow) and the MCP joints of the index, ring,

and little fi ngers (arrowheads) Fusiform soft tissue swelling is present

at the PIP joint of the ring fi nger (long arrow).

FIGURE 12.2 Rheumatoid arthritis with early erosive changes at the

MCP joints

also helpful in the evaluation of the complications of rheumatoid

arthritis at the craniocervical junction and elsewhere

Hand and Wrist

There is considerable variability in the distribution of

radio-graphic abnormalities in rheumatoid arthritis, and the fi ndings on

radiographs may not correlate with the clinical features The earliest

radiographic changes are fusiform soft-tissue swelling and

juxta-articular osteoporosis (Figs 12.1 and 12.2) In the hand,

rheuma-toid arthritis classically involves the MCP and PIP joints The earliest

bone erosions are generally at the MCP joints (Fig 12.3), often the

second and third on the radial side The PIP joint of the middle fi

n-ger is another site of typical early involvement Oblique radiographs

may show subtle subchondral bone resorption Fusiform soft-tissue

swelling, juxta-articular osteoporosis, concentric loss of cartilage

space, and acute marginal erosions may be seen (Fig 12.4)

Compres-sive erosions and remodeling of bone may result from the collapse

of osteoporotic bone by muscle tension; this is especially common

at the MCP joints Loss of the normal balanced tension at the digits

results in various alignment deformities, including the swan neck

and boutonniere deformities of the fi ngers (see Fig 11.15) and the

Z-shaped deformity of the thumb (Fig 12.5) Superfi cial erosions

of the cortex may occur beneath the infl amed tendon sheaths,

espe-cially along the outer aspect of the distal ulna, the dorsal aspect of

the fi rst metacarpal, and the proximal phalanx of the fi rst digit

In the wrist, pancompartmental involvement is usual (Fig 12.6)

The earliest bone changes are erosions at the ulnar and radial styloid processes and at the waists of the capitate and scaphoid bones On MRI, erosions are evident as focal defects in the bone that are low to intermediate signal on T1-weighted images and high signal on T2-weighted images (Fig 12.7) On T1-weighted images after gadolinium enhancement, the pannus within the ero-sions enhances Malalignment in advanced disease results from loss of balanced muscular tension and ligamentous restriction

Involvement of tendons can be demonstrated by MRI (Fig 12.8)

On T2- weighted images, synovial sheaths show fl uid and high signal On T1-weighted images after the gadolinium injection, the infl amed synovium shows enhancement The posttraumatic liga-mentous instability patterns of the wrist described in Chapter 2 are often seen in advanced rheumatoid arthritis

Other Peripheral Joints

In the elbow, synovial hypertrophy and effusion provide a fat pad sign As in other joints, periarticular osteoporosis, uniform joint space narrowing, and erosions are seen In the glenohumeral joint, erosions are especially prominent around the proximal humerus, and rotator cuff tear or atrophy causes superior subluxation of the humeral head and adaptive changes in the inferior surface of the acromion from the humeral head (Figs 12.9 and 12.10) Resorption

of the distal clavicle and widening of the acromioclavicular joint are

FIGURE 12.3 Rheumatoid arthritis involving the MCP joint of the ring fi nger A: Radiograph shows early

sub-chondral bone erosion (arrow) B: Coronal T2-weighted fat-suppressed MRI shows effusion (arrow) C: Coronal

T1-weighted fat-suppressed MRI following gadolinium injection shows enhancement (arrow).

FIGURE 12.4 Rheumatoid arthritis with juxta-articular osteoporosis.

frequently observed in rheumatoid arthritis In the knee, meniscal

invasion by pannus occurs early and may be detectable on MRI

Typical infl ammatory changes may be superimposed on

second-ary degenerative changes, but the proliferative bone response is

disproportionately modest in comparison to the loss of joint space

(Fig 12.11) On MRI, effusions, erosions, diffuse cartilage loss,

bone marrow edema, and pannus may be demonstrated at the knee

(Fig 12.12) The hip is less frequently involved than the knee

Con-centric uniform loss of joint space with axial migration is usual, but

superior migration similar to that in osteoarthritis may also occur

FIGURE 12.5 Hand deformities in rheumatoid arthritis PA

radio-graph shows boutonniere deformity of the ring fi nger, Z-shaped mity of the thumb, proximal dislocation of the fi rst CMC joint, volar dislocation of the MCP joint of the little fi nger, and ulnar translocation

defor-of the carpus

FIGURE 12.7 Rheumatoid arthritis involving the carpal bones A: Coronal T1-weighted MRI shows erosions

B: Coronal T1-weighted fat-suppressed MRI following gadolinium injection shows enhancement in the erosions,

corresponding to infl ammatory pannus

FIGURE 12.6 Rheumatoid wrist A: Early fi ndings include juxta-articular osteoporosis and subtle erosions,

including the scaphoid waist (arrow) B: The same patient 6 years later has severe erosions and subluxations Ulnar

translocation is present The bones are diffusely osteoporotic, with no proliferative changes The scaphoid waist

erosion has become large (arrow).

Acetabular protrusion (protrusio acetabuli), fi brous ankylosis,

subchondral cysts, erosions, and secondary reparative and

degen-erative changes are common If steroids are administered,

osteone-crosis of the femoral head is a potential complication In the foot,

changes may be seen early at the metatarsophalangeal (MTP) and

interphalangeal (IP) joints of the great toe (Fig 12.13) Although

the usual changes of rheumatoid arthritis that are found elsewhere

in the skeleton may be present in the foot, erosions tend to be small

and infrequent Soft-tissue involvement may lead to hallux valgus

and planovalgus deformity of the foot In the heel, retrocalcaneal bursitis, Achilles tendonitis, and plantar fasciitis may cause swelling and calcaneal erosions (Fig 12.14) Spontaneous Achilles tendon rupture may occur

Spine

In the spine, the upper cervical spine is the only common site of involvement As many as 70% of patients with rheumatoid arthritis

FIGURE 12.9 Radiograph of the shoulder in advanced rheumatoid

arthritis shows osteopenia, erosion of the distal clavicle, and

remodel-ing of the undersurface of the acromion and medial humeral shaft

FIGURE 12.10 Rheumatoid shoulder with osteoporotic bones and

secondary glenohumeral degenerative change The distal clavicle is eroded and remodeled

FIGURE 12.8 Rheumatoid arthritis of left ankle with tenosynovitis

Axial T1-weighted fat-suppressed MRI following gadolinium

admin-istration shows thickened synovium with intense uptake (arrowhead)

Effusion (e) is noted in the anterior ankle, and longitudinal split tears of

the posterior tibialis tendon (white arrow) and peroneus brevis tendon

(black arrows) are noted.

are affected symptomatically at some time, and up to 85% of those

with classic rheumatoid arthritis have radiographic changes at the

upper cervical spine The atlantoaxial articulation (C1–2) has a

synovial joint anteriorly where the odontoid process articulates

with the anterior arch of C1 and is stabilized posteriorly by the transverse ligament A bursa is interposed between the odontoid process and the transverse ligament Synovitis at these sites may cause erosions of the odontoid process and rupture of the trans-verse ligament (Figs 12.15 and 12.16), resulting in a widened predental interval One consequence is atlantoaxial instability, with imminent danger of quadriplegia or death Below the level

of C2, the cervical spine may be diffusely involved by joint space narrowing Infl ammatory pannus at the synovial uncovertebral joints (joints of Luschka) may extend into the intervertebral disks

The thoracic spine and lumbar spine are usually spared Sacroiliac (SI) joint involvement is infrequent and, when present, is mild and asymmetric

Extra-Articular Manifestations

Extra-articular manifestations of rheumatoid arthritis include rheumatoid nodules, development of cutaneous fi stulas, infections, hematologic abnormalities, vasculitis, renal disease, pulmonary dis-ease, and cardiac complications

CONNECTIVE TISSUE DISEASE

Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a chronic systemic disease, the pathogenesis of which is related to immune complex deposi-tion It is more common in women by an 8:1 ratio, and there is a component of genetic susceptibility The fl uorescent ANA test is virtually always positive at the onset of clinical disease Manifesta-tions in the musculoskeletal system are common and may precede other systemic manifestations by months or years Nonerosive symmetric polyarthritis with a distribution similar to that of rheu-matoid arthritis is present in 75% to 90% of patients with SLE

Early fi ndings on radiographs are fusiform soft-tissue swelling and juxta-articular osteoporosis, but there should be no joint space

FIGURE 12.12 Rheumatoid knee A: Sagittal T2-weighted fat-suppressed MRI shows large effusion and Baker

cyst with synovial thickening (arrows) Diffuse cartilage loss and subchondral edema are present B: Coronal

T1-weighted fat-suppressed MRI following gadolinium shows synovial and subchondral enhancement

FIGURE 12.11 Rheumatoid knees The bones are osteoporotic Uniform joint space loss is present with minimal

proliferative bone changes Some secondary osteoarthritic changes are present in the lateral compartment of the left knee

narrowing or erosions A deforming nonerosive arthropathy is also

common in SLE The hands are typically involved at the MCP and

IP joints (Figs 12.17 and 12.18) Thumb, wrist, and foot

involve-ment are more common than shoulder and knee involveinvolve-ment,

and 10% of patients may develop atlantoaxial subluxation These

deformities are initially reducible, and radiographs may be

nor-mal Fixed deformities and secondary degenerative changes may

develop with time Osteonecrosis may involve the femoral head,

femoral condyle, humeral head, and other sites, and commonly

has a symmetric distribution Myositis, tendon weakening and spontaneous rupture, and soft- tissue calcifi cation are other mus-culoskeletal manifestations

Scleroderma

Scleroderma (progressive systemic sclerosis) is a multisystem

fi brosing autoimmune connective tissue disease of variable cal course Characteristically, the skin becomes fi brotic, thickened,

clini-are common in the phalangeal tufts (Fig 12.19) Soft-tissue atrophy results in cone-shaped fi ngertips Subcutaneous calcifi ca-tions are typically present in multiple digits and elsewhere in the extremities; the calcium deposits are dystrophic and consist of cal-cium hydroxyapatite deposits at sites of local tissue damage Cal-cifi cation may also occur in tendons and tendon sheaths, in joint

FIGURE 12.13 Rheumatoid foot The great toe is deviated

later-ally, and the remaining MTP joints are subluxated Erosions are

pres-ent at all of the MTP joints and the IP joint of the great toe; the other

joints appear spared Some erosions appear sclerotic, suggesting clinical

quiescence

FIGURE 12.14 Rheumatoid arthritis Swelling of the

retrocalca-neal soft tissues is present with a large erosion in the adjacent bone

(arrow).

FIGURE 12.15 Rheumatoid arthritis Atlantoaxial subluxation is

present with a wide gap between the anterior arch of C1 and the

odon-toid process (arrow).

FIGURE 12.16 Rheumatoid arthritis Sagittal T2-weighted MRI

shows pannus (arrow) eroding the odontoid process and causing mass

effect on the spinal cord

and taut Gastrointestinal and renal involvement is prominent

Radiologic manifestations in the musculoskeletal system are

present in most patients These abnormalities are usually seen in

the hands and consist of soft-tissue atrophy, soft-tissue calcifi

ca-tion, resorption of the phalangeal tufts, and distal

interphalan-geal (DIP) joint erosions Osseous destruction and bony erosions

FIGURE 12.17 Systemic lupus erythematosus with alignment deformities A, B: Lateral and PA radiographs

show swan neck deformities of the ring and little fi ngers, with PIP hyperextension of the middle fi nger

FIGURE 12.18 Systemic lupus erythematosus with severe

sublux-ations Erosions are absent

FIGURE 12.19 Scleroderma with calcium hydroxyapatite deposits in

the thumb and atrophy of the soft tissues

capsules, and even within the joint cavity Synovial fi brosis without

infl ammation may cause fl exion contractures

Dermatomyositis and Polymyositis

Dermatomyositis and polymyositis are diseases of unknown etiology

affecting the striated muscle by diffuse, nonsuppurative infl

amma-tion and degeneraamma-tion The pathogenesis involves an autoimmune

mechanism In dermatomyositis, the skin is also involved Multiple

clinical classifi cations are based on various features, particularly

progressive muscle weakness and rash There is an associated

risk of malignancy in patients older than 40 years of age with

dermatomyositis, especially men The diagnosis is made by serum enzyme studies, electromyography, and muscle biopsy Early imag-ing fi ndings of dermatomyositis and polymyositis can be made on MRI T2-weighted MRI shows high signal in the involved muscles (Fig 12.20) Involvement is generally symmetric bilaterally, and the course of the disease can be followed by MRI On radiographs, the characteristic abnormality is widespread soft-tissue calcifi cation, particularly of intermuscular fascial planes between large proximal limb muscles (Figs 12.21 and 12.22) There may also be subcuta-neous calcifi cations similar to those in scleroderma (Fig 12.23)

Muscle atrophy, contractures, and chronic osteoporosis are fi ndings late in the clinical course

FIGURE 12.20 Dermatomyositis A: Axial STIR MRI shows muscle edema (high signal) symmetrically

dis-tributed in the gluteal and adductor muscles B: Axial T1-weighted fat-suppressed MRI following intravenous

gadolinium shows enhancement that corresponds to the regions of edema

FIGURE 12.21 Dermatomyositis at the ankle with soft-tissue

calcifi cation

FIGURE 12.22 Dermatomyositis at the knee with prominent

soft-tissue calcifi cation around the quadriceps muscles

FIGURE 12.23 Polymyositis with soft-tissue calcifi cation (arrow)

involving the index fi nger

FIGURE 12.24 Ankylosing spondylitis A: AP radiograph of the lumbar spine shows that the SI joints and the

posterior elements of the spine (arrow) are ankylosed B: Lateral radiograph of the lumbar spine shows squaring

(arrows) of the anterior aspects of the lumbar vertebral bodies and ankylosis of the posterior elements.

The radiographic features of disease may also overlap so that an individual case may show combinations of features of rheumatoid arthritis, scleroderma, SLE, and dermatomyositis These overlap

syndromes may also be called mixed connective tissue disease.

SPONDYLOARTHROPATHY

The spondyloarthropathies are a heterogeneous group of related conditions Musculoskeletal manifestations common to these diseases include spinal involvement, especially of the SI joints, enthesopathy, and asymmetric peripheral arthritis of the lower limbs Additional common features are genetic predisposition;

inter-extra-articular manifestations in the skin, gut, urogenital tract, or eyes; negative serum RF; and an association with HLA-B27 These

conditions have in the past been called rheumatoid variants to tinguish them from rheumatoid arthritis and seronegative spondy-

dis-loarthropathy to refl ect the negative serum RF.

Ankylosing Spondylitis

Ankylosing spondylitis is a chronic infl ammatory disease of the spine and SI joints The etiology is unknown, but there is a genetic component; 90% to 95% of white patients with classic ankylosing spondylitis have HLA-B27 (compared with 9% of all white patients)

Symptomatic disease affects approximately 1% of the general population; the prevalence of severe disease is approximately 0.1%

The typical onset is insidious lower back pain and stiffness in lescent men In the severe classic form, there is gross ankylosis and deformity of the spine; in mild forms, there may be only occasional arthralgias In most cases, ankylosing spondylitis is a benign, self-limited, and undiagnosed disease with absent or minimal radio-graphic changes The overall sex distribution is probably equal, but men generally have severe, progressive disease, whereas women have mild, self-limited disease

ado-Overlap Syndromes

Patients may have rheumatic diseases with clinical features that

overlap those of several of the more well-defi ned rheumatoid

diseases, particularly at the beginning or end of the clinical course

FIGURE 12.25 Ankylosing spondylitis of the cervical spine Lateral

radiograph shows syndesmophytes (arrow) bridging C2 through C4

vertebral bodies

FIGURE 12.26 Ankylosing spondylitis with syndesmophytes and

ossifi cation of the posterior ligamentous structures The SI joints have

fused

Ankylosing spondylitis begins in the lumbosacral region and

ascends to the cervical spine Radiographically, the involved

verte-bral bodies become squared off by erosions from infl ammation in

the prevertebral soft tissues (Fig 12.24) The facet joints become

infl amed and then fused, and syndesmophytes—ossifi cations in and

around the periphery of the annulus fi brosus—form at multiple contiguous levels, eventually leading to a spine that looks like bam-boo (Figs 12.25 and 12.26) Back pain diminishes or disappears as the spine fuses, but the fused spine becomes osteoporotic, fragile, and subject to insuffi ciency fractures In the pelvis, the SI joints become symmetrically blurred, sclerotic, and fused (Fig 12.27)

Early in this process, the SI joints have subchondral granulation tissue, and the joint cartilage becomes replaced by fi brous tissue

Ankylosis follows the formation of new cartilage and bone in the joint space

Approximately 20% of patients with ankylosing tis present initially with peripheral polyarthritis, and, ultimately, approximately 35% will have peripheral disease This peripheral

spondyli-FIGURE 12.27 Ankylosing spondylitis with symmetric, infl

amma-tory arthritis of the hips, ankylosis of the SI joints, and hyperostosis at the ischial rami

FIGURE 12.28 Ankylosing spondylitis with traumatic cervical spine

fracture at C5–6 (arrow).

FIGURE 12.29 Reactive arthritis with sacroiliitis, greater on the left

than the right (arrow).

polyarthritis is similar to rheumatoid arthritis in clinical

manifestations, radiographic appearance, and pathophysiology, but

the distribution of disease tends to be different Feet, ankles, knees,

hips, and shoulders are typically involved in an asymmetric fashion;

the hands are usually spared Permanent stiffness or bony

ankylo-sis is likely Peripheral polyarthritis may precede, coincide with, or

follow the onset of spinal manifestations

MRI has proved more sensitive than radiography in the early

detection of sacroiliitis T1-weighted fat suppression with

gado-linium administration and fast inversion recovery are superior to

T1- and T2-weighted images MRI fi ndings of sacroiliitis include

abnormal cartilage signal intensity, erosions, increased intensity

in the joint, and subchondral bone marrow edema MRI may also

be able to distinguish sacroiliitis due to spondyloarthropathy from

septic arthritis of the SI joint

One major orthopedic complication of ankylosing spondylitis

is increased biomechanical fragility of the spine Syndesmophytes

bridging the vertebral bodies and ankylosis of the posterior

ele-ments result in a stiff spine that cannot move or dissipate traumatic

forces Bony remodeling of an ankylosed spine does not improve

its biomechanical strength as a unit When patients with

ankylos-ing spondylitis are involved in falls or other accidents, fractures and

fracture dislocations of the spine are common (Fig 12.28) These

fractures may progress to nonunion

Reactive Arthritis

Reactive arthritis is an acute infl ammatory arthritis that follows

an infection elsewhere in the body, but infectious

organ-isms cannot be cultured from the joint fl uid or synovium The

pathogenesis of the disease is thought to be immunologic in

nature, with a genetic predisposition After gastrointestinal

infec-tions by Shigella, Salmonella, Yersinia, or Campylobacter, or a

genitourinary infection with Chlamydia, approximately 1% to

4% of patients develop reactive arthritis Although the triad of

peripheral arthritis, conjunctivitis, and urethritis has been

clas-sically associated with reactive arthritis, the current defi nition

generally includes cases of arthritis that occur within 2 months of

an episode of venereal infection or epidemic dysentery The

clas-sic triad is present in only one third of cases of reactive arthritis

The diagnosis may be diffi cult to make because there is no defi

-nite laboratory test, and the dysenteric or venereal episode may be

mild or silent There is a marked male predominance of at least

5:1 The typical age of onset is 15 to 40 years HLA-B27 is present

in 70% to 80% of cases, and the serum RF is negative Clinically,

reactive arthritis is an asymmetric lower extremity

oligoarthri-tis manifested by sausage digits, heel pain and swelling, low back

pain, and SI joint tenderness Early clinical signs include

effu-sion, periarticular edema, bursitis, and tendinitis Fluffy

periosti-tis, enthesopathy, paravertebral comma-shaped ossifi cation, and

asymmetric sacroiliitis often develop Bone density is preserved

in chronic disease

Radiographic abnormalities develop in 60% to 80% of cases,

with involvement of synovial joints, symphyses, and entheses The

disease has a predilection for the foot—especially the great toe,

ankles, knees, and SI joints—and manifestations are rarely seen

above the level of the umbilicus Bony erosions combined with

bony proliferation characterize an asymmetric arthritis Erosions

fi rst appear at the joint margins and may progress to involve the

subchondral bone in the central portion of the articulation Bony

proliferation may take the form of periostitis (linear or fl uffy), calcifi cation and ossifi cation at entheses, and intra-articular bone production with bony ankylosis Additional abnormalities may include fusiform soft-tissue swelling, effusions, regional or peri-articular osteoporosis, and symmetric and concentric joint space narrowing

Sacroiliitis is the most common manifestation The incidence

of sacroiliitis increases with the chronicity of the disease, rising from 5% to 10% of cases at onset to perhaps 75% after several years

Sacroiliitis is evident on radiographs as blurring and eburnation of the adjacent sacral and iliac articular surfaces, initially worse on the iliac side (Fig 12.29) Bilateral changes are typical, and these may be symmetric or asymmetric

Spinal involvement in reactive arthritis is much less frequent than in ankylosing spondylitis or psoriasis Asymmetric paraver-tebral ossifi cation about the lower three thoracic and upper three lumbar vertebrae in reactive arthritis is indistinguishable from the corresponding changes in psoriatic spondylitis These ossifi cations are thought to result from infl ammatory changes in the paraver-tebral connective tissue that lead to calcifi cation and ossifi cation

Unlike ankylosing spondylitis, squaring of the vertebral bodies, facet joint erosion, sclerosis, and osseous fusion are unusual in reac-tive arthritis

a form of reactive arthritis incited by streptococcal and coccal infection of psoriatic plaques and affected nails HLA-B27 is

found in 60% to 80% of patients with psoriatic spondylitis but in

only 20% of patients with psoriatic peripheral arthritis Serum RF

is absent Psoriatic arthritis has fi ve patterns of clinical

presenta-tion: (a) asymmetric oligoarthritis, seen in more than 50% of cases;

(b) polyarthritis with predominantly DIP joint involvement, the

classic presentation, which is seen in 5% to 19%; (c) symmetric

seronegative polyarthritis simulating rheumatoid arthritis, seen in

up to 25%; (d) sacroiliitis and spondylitis resembling ankylosing

spondylitis, seen in 20% to 40%; and (e) arthritis mutilans with

resorption of phalanges, seen in 5% Individual patients may change

from one clinical pattern to another Two thirds of patients have an

insidious onset, whereas one third have an acute onset mimicking

gout or septic arthritis The age of onset is 35 to 45 years, and there

is no sex predominance

The predominant radiologic abnormalities are found

asym-metrically in the upper extremities and result from a synovitis

that is similar in pathophysiology to rheumatoid arthritis The

distribution of articular involvement in the hands tends to

be distal, commonly the DIP joints of the fi ngers, and usually

accompanies fi ngernail involvement Soft-tissue swelling of the

digits tends to be of the “sausage” variety, in which the entire

digit is swollen, not just the joints (Fig 12.30) Dramatic joint

space loss to the point of erosion and resorption of the

articulat-ing ends of bones may occur Pencil-in-cup erosions (Fig 12.31)

and periosteal bony excrescences (Fig 12.32) are other typical

fi ndings The arthritis is highly erosive and in the hands or feet

may lead to arthritis mutilans, which is severe resorptive arthritis

of the phalanges (Figs 12.33 and 12.34) In the spine, irregular,

asymmetric paravertebral excrescences of the bone appear; these

may be quite bulky and merge with the underlying vertebral

bod-ies and disks (see Fig 11.20) The changes in the spine and SI

joints in psoriatic arthritis tend to be more marked than in

reac-tive arthritis, but they are often indistinguishable Sacroiliitis may

progress to ankylosis

FIGURE 12.30 Psoriatic arthritis with “sausage digit” swelling,

ero-sions (long arrow), and periostitis (short arrow) of the index fi nger. FIGURE 12.31 Psoriatic arthritis with interdigitating erosions

(pencil-in-cup appearance)

FIGURE 12.32 Psoriatic arthritis with infl ammatory periostitis.

FIGURE 12.33 Psoriatic arthritis involving the foot The IP joint

of the great toe is severely eroded, as are the DIP joints of the third

through fi fth toes

FIGURE 12.34 Arthritis mutilans presentation of psoriatic arthritis

in the hand and wrist The DIP and PIP joints of all of the fi ngers are

severely involved There is pancompartmental involvement of the wrist,

with erosions and mature periosteal bone

FIGURE 12.35 Unilateral infl ammatory sacroiliitis in a patient with

infl ammatory bowel disease Axial CT scan shows erosions of the left SI

joint (arrows).

of patients with Crohn disease may have bilateral sacroiliitis, and 25% of these develop ankylosing spondylitis The sacroiliitis and spondylitis tend to be progressive and not particularly related to the bowel disease (Fig 12.35) Certain dysenteric infections are associ-ated with reactive arthritis, as discussed earlier in this chapter

Differential Diagnosis

Although the spondyloarthropathies have common features, it

is frequently possible to distinguish one from the other in vidual patients (Table 12.1) The manifestations of ankylosing spondylitis are usually severe in the spine and SI joints and less severe in the peripheral joints The manifestations of psoriatic arthritis are usually severe in the small peripheral joints and less severe in the large peripheral joints, spine, or SI joints The mani-festations of reactive arthritis are usually mild and rarely involve the upper body When disease is mild and radiographic fi ndings are minimal, it may be diffi cult to recognize a specifi c form of spondyloarthropathy

JUVENILE IDIOPATHIC ARTHRITIS

Juvenile idiopathic arthritis is a heterogeneous group of idiopathic infl ammatory joint conditions that have in common (1) involve-ment for 6 weeks or more and (2) onset before 16 years of age

This classifi cation by the International League for Rheumatology (Table 12.2) has replaced older classifi cations of “juvenile rheuma-toid arthritis” and “juvenile chronic arthritis.” The radiologic fi nd-ings in juvenile idiopathic arthritis refl ect the effect of a chronic infl ammatory arthritis on a growing skeleton and are generally not specifi c for a particular clinical entity The radiologic features include synovitis, soft-tissue swelling, osteoporosis, periostitis, erosions, ankylosis, and growth disturbances (Fig 12.36) The earlier the age of onset, the more severe the fi ndings Not all fi nd-ings are likely to be present together, but combinations of these

fi ndings may point to the diagnosis The disease may remit in adulthood, but permanent muscle wasting, growth deformities from epiphyseal overgrowth and early growth plate closure, loss

of function from ankylosis and joint contractures, and secondary osteoarthritis are common sequelae (Fig 12.37) Compared with

similar to rheumatoid arthritis The peripheral arthritis may wax

and wane in tandem with exacerbations and remissions in the bowel

disease Sacroiliitis and spondylitis resembling or identical to

anky-losing spondylitis may also occur in ulcerative colitis Up to 20%

TAB LE 12.1 Distinguishing Features of Spondyloarthropathy

Feature Ankylosing Spondylitis Reactive Arthritis Psoriatic Arthritis

Clinical setting Low back pain, adolescents Following dysenteric or venereal

infection

PsoriasisSex predominance Male (classic disease) Male None

Joint distribution SI, entire spine SI, lumbar spine, feet Hands, feet, thoracolumbar spine

Severity of involvement Severe ankylosis Mild Severe erosions

SI joint involvement Bilateral, symmetric sacroiliitis

invariably leading to ankylosis

Bilateral, asymmetric sacroiliitis Bilateral, asymmetric sacroiliitis

may progress to ankylosisType of phytes Delicate syndesmophytes Paravertebral ossifi cation Paravertebral ossifi cation

TAB LE 12.2 Frequency of Clinical Types of Juvenile Idiopathic Arthritis

Clinical Type Frequency (%)

Oligoarthritis (one to four joints) 45Persistent

ExtendedPolyarthritis (fi ve or more joints)

Enthesis-related arthritis 10Psoriatic arthritis 13

Source: Johnson K, Gardner-Medwin J Childhood arthritis: Classifi cation and radiology Clin Radiol

2002;57(1):47–58

FIGURE 12.36 Juvenile idiopathic arthritis in the hands A: Left side shows the bones are osteopenic Soft-tissue

swelling is evident at all of the joints Periostitis is present (arrow) The articular margins of the bones are eroded

and small B: Right side shows similar fi ndings.

FIGURE 12.37 Sequelae of juvenile idiopathic arthritis in a young adult A: The hand has short bones whose

growth plates fused prematurely B: Intra-articular tarsal fusions are present; the bones are osteoporotic.

FIGURE 12.38 Juvenile idiopathic arthritis involving the hips

Radiograph shows diffuse joint space narrowing, secondary dysplasia,

and superimposed degenerative changes

radiography, MRI and sonography are more sensitive imaging

indicators of disease activity and can demonstrate synovitis,

ero-sions, and articular cartilage status MRI can also demonstrate

bone marrow edema

Symmetric involvement occurs in the systemic arthritis, seronegative and seropositive polyarthritis, and extended oligoar-thritis forms of juvenile idiopathic arthritis Typical sites of involve-ment may include the MCP and IP joints of the hand, the wrist, elbow, hip (Fig 12.38), knee, ankle, foot, and cervical spine In the hand, common fi ndings include soft-tissue swelling, osteoporosis, bony ankylosis, periostitis, growth disturbances, epiphyseal com-pression fractures, and joint subluxation Asymmetric involvement occurs in the persistent oligoarthritis, enthesis-related arthritis, and psoriatic arthritis forms of juvenile idiopathic arthritis Unlike adult forms of infl ammatory arthritis, monarticular onset in a knee appears to be a common presentation for all forms of juvenile idiopathic arthritis (Fig 12.39)

SEPTIC ARTHRITIS

Septic arthritis is usually caused by nongonococcal bacteria in small children or elderly adults Infections of joints usually fol-low hematogenous spread of organisms to the synovium from

a preexisting infection in a remote site Less commonly, adjacent osteomyelitis extends into a joint, or, rarely, a penetrating wound introduces organisms The most common infecting organism in

adults is Staphylococcus aureus The most common organism in infants is beta-hemolytic Streptococcus and in preschool-aged chil- dren, Haemophilus infl uenzae In patients with a chronic underly-

ing disease such as diabetes or alcoholism, Gram-negative bacteria are a common cause of septic arthritis in those with concurrent

genitourinary tract infections, and Streptococcus pneumoniae is a

common cause in those with concurrent lung infections Other risk

FIGURE 12.39 Juvenile idiopathic arthritis in a 4 year old Effusion is evident, but the disease is of too recent onset

to have caused developmental effects The appearance is nonspecifi c A: Lateral radiograph B: AP radiograph.

factors for septic arthritis include rheumatoid arthritis, SLE, total

joint replacement, and old age

From the initial site of infl ammation and microabscess

forma-tion in the synovium, the infecforma-tion may spread to the joint space,

bones, and soft tissues Proteolytic enzymes released into the joint

space by synovial cells and activated PMNs destroy the ground

substance and then the collagen framework of the articular

carti-lage Destruction of the joint takes only a few days The usual

clini-cal presentation is the abrupt onset of pain in a swollen, tender,

infl amed joint Nonspecifi c physical and laboratory signs of local

and systemic infection may be present, but a preexisting source of

infection is not always obvious The diagnosis is made by

arthrocen-tesis; injection of contrast medium under fl uoroscopy can confi rm

intra-articular needle placement when necessary The joint fl uid is

opaque, with a cell count of more than 100,000 WBC/mm3, a

dif-ferential with more than 85% PMNs, and a glucose level that is at

least 50 mg/dL less than the concurrent serum level Cultures of the

fl uid are almost always positive, and blood cultures are positive in

50% of cases The knee is the most common site On radiographs,

acute septic arthritis is evident as soft-tissue swelling and effusion

Juxta-articular osteoporosis develops, and within 7 to 10 days, the

articular cartilage is gone, and the joint space is narrowed Findings

in young children may be subtle, and sonography (to look for

effu-sion) or MRI (to look for effusion and osteomyelitis) may be helpful

(Fig 12.40) Prolonged antibiotic treatment and surgical drainage

are often required, but the joint is usually destroyed despite

treat-ment Secondary degenerative changes ultimately develop

Gonococcal arthritis occurs among sexually active young

adults, especially women (80% of cases), and is the most common

infectious arthritis in this age group Preexisting HIV infection is a

risk factor Hematogenous dissemination of the organism causes

fever and arthralgias, typically evident 2 weeks after the initial

infection Polyarticular and asymmetric involvement is usual, and there is a predilection for the knees, wrists, and ankles Arthrocen-tesis fl uid cultures are positive in fewer than 25% of cases, but the response to antibiotics is rapid, and the outcome is good in nearly all cases Radiographs may show only joint effusion and soft-tissue swelling

FIGURE 12.40 Septic arthritis in a child Axial T2-weighted

fat-suppressed MRI shows large left hip effusion distending the capsule

(arrow) and subluxating the femoral head (H).

MISCELLANEOUS

Granulomatous Synovitis

Tuberculosis, atypical mycobacteria, and fungi may spread to the

joints, resulting in a granulomatous synovial infection that requires

synovial biopsy or joint aspiration for diagnosis These are chronic,

insidiously destructive processes In the usual situation, the

under-lying infection is in the lung, the process is monarticular, and there

is osteomyelitis adjacent to the involved joint On radiographs,

osteopenia is prominent, and osteolysis with little or no reactive

bone formation is characteristic (Fig 12.41) A large joint effusion

may be present These infections have become progressively less

rare in the United States since the beginning of the HIV epidemic

(see Chapter 16)

Viral Synovitis

Viral synovitis (toxic synovitis) is transient and self-limited in

nearly all cases The synovitis may be caused by direct viral infection

of the synovium or by the deposition of immune complexes in the

synovium as a systemic viremia is cleared The viruses associated

with arthritis include hepatitis B, rubella, enterovirus, adenovirus,

varicella-zoster, Epstein-Barr, cytomegalovirus, and herpes simplex

No specifi c treatment is available or necessary, but aspiration of the joint may be indicated in children to exclude bacterial infection

Lyme Disease

Lyme disease is an infl ammatory multisystem disease that

fol-lows infection by the spirochete Borrelia burgdorferi The vector

is the deer tick, an insect endemic to forested areas of the United States, Europe, and Australia Clinical fi ndings in the acute infec-tion include a rash and fl ulike syndrome Months later, multisystem involvement may become apparent In the musculoskeletal system, arthralgias of sudden onset and short duration appear, sometimes migratory and recurrent One or more joints may be involved, most frequently the large joints, but also the temporomandibular and SI joints and the hands and feet The radiographic appearance is non-specifi c and may include peripheral enthesopathy and periostitis

Occasionally, a chronic infl ammatory oligoarthritis that resembles rheumatoid arthritis develops, particularly in the knees

SOURCES AND READINGS

Arnett FC, Edworthy SM, Bloch DA, et al The American Rheumatism ciation 1987 revised criteria for the classifi cation of rheumatoid arthritis

Asso-Arthritis Rheum 1988;31:315–324.

Brower AC Arthritis in Black and White 2nd Ed Philadelphia, PA: WB

Saunders; 1997

eMedicine http://emedicine.medscape.com

Firestein GS, Budd RC, Harris ED Jr, et al Kelley’s Textbook of Rheumatology

8th Ed Philadelphia, PA: Saunders; 2008

Forrester DM, Brown JC The Radiology of Joint Disease 3rd Ed

Philadel-phia, PA: WB Saunders; 1987

Griffi n LY Essentials of Musculoskeletal Care 3rd Ed Rosemont, IL:

Ameri-can Academy of Orthopedics; 2005

Jacobson JA Fundamentals of Musculoskeletal Ultrasound Philadelphia, PA:

Saunders; 2007

Johnson K, Gardner-Medwin J Childhood arthritis: Classifi cation and

radi-ology Clin Radiol 2002;57(1):47–58.

Koopman WJ, Boulware DW, Heudebert G Clinical Primer of Rheumatology

Philadelphia, PA: Lippincott Williams & Wilkins; 2003

Koopman WJ, Moreland LW, eds Arthritis and Allied Conditions: A Textbook

of Rheumatology 15th Ed Philadelphia, PA: Lippincott Williams &

Wilkins; 2004

Martino F, Silvestri E, Grassi W, Garlaschi G Musculoskeletal Sonography:

Technique, Anatomy, Semeiotics and Pathological Findings in Rheumatic Diseases Berlin: Springer; 2007.

Oostveen JC, van de Laar MA Magnetic resonance imaging in rheumatic

disorders of the spine and sacroiliac joints Semin Arthritis Rheum

2000;30:52–69

Resnick D, ed Diagnosis of Bone and Joint Disorders 4th Ed Philadelphia,

PA: Saunders; 2002

Sommer OJ, Kladosek A, Weiler V, Czembirek H, Boeck M, Stiskal M

Rheumatoid arthrits: A practical guide to state-of-the-art imaging,

image interpretation, and clinical implications Radiographics 2005;

25:381–398

Sugimoto H, Takeda A, Hyodoh K Early-stage rheumatoid arthritis:

Pro-spective study of the effectiveness of MR imaging for diagnosis

Radiol-ogy 2000;216:569–575.

FIGURE 12.41 Tuberculous arthritis Radiograph of the thumb

shows destruction of the MCP joint (arrow) with osteoporosis and

minimal reactive bone formation

13 Noninfl ammatory Joint Disease

Calcium Pyrophosphate Dihydrate

Crystal Deposition Disease

Hydroxyapatite Deposition Disease

Gout

Metabolic Deposition DiseaseTophaceous GoutMulticentric ReticulohistiocytosisAmyloid Arthropathy

Miscellaneous Joint ConditionsPigmented Villonodular SynovitisSynovial ChondromatosisSynovial HemangiomatosisBaker Cyst

Posttraumatic Osteolysis of the Distal Clavicle

Degenerative Foot ConditionsFlatfoot (Pes Planus)Calcaneus

Great ToeLesser ToesIntervertebral Disk DegenerationDiffuse Idiopathic Skeletal HyperostosisBaastrup Disease

T his chapter covers joint diseases that have predominantly noninfl ammatory features on radiographs

OSTEOARTHRITIS

Osteoarthritis (degenerative joint disease) is a form of joint disease

characterized by degenerative changes involving synovial joints

Osteoarthritis can be divided into primary and secondary types, but

the division is artifi cial: The underlying cause is evident in

second-ary osteoarthritis but not in primsecond-ary or idiopathic osteoarthritis

The distinction has some practical value in understanding the

pro-cess and planning clinical management Osteoarthritis is the most

common form of arthritis Its prevalence increases with age, so that

osteoarthritis is nearly ubiquitous in patients older than 65 years of

age Up to 45 years of age, it is more prevalent in men; from 45 to

55 years of age, the prevalence is equal; and after 55 years of age,

it is more prevalent in women The most common presentation of

osteoarthritis is joint pain and limitation of activity Laboratory tests

are used to eliminate other forms of arthritis as clinical possibilities

Primary Osteoarthritis

The early morphologic abnormality in primary osteoarthritis is

fi brillation of the articular cartilage The surface develops fi bril-like

projections and becomes irregular Underlying this morphologic

change is disruption at the molecular level of the superfi cial

armor-plate layer and collagen framework, resulting in progressive loss of

proteoglycans from the ground substance and collagen from the

framework Chondrocytes increase protein synthesis, presumably

in response to the continuing loss of structural components

Pro-gressive erosion and formation of fi ssures in the surface eventually

expose the subchondral bone The initial event that incites fi

bril-lation of the cartilage surface is unknown; some forms of primary

osteoarthritis may result from an initial alteration in articular

car-tilage physiology

Radiographic fi ndings do not appear in osteoarthritis until articular cartilage loss results in secondary adaptive changes in bone These fi ndings include uneven loss of articular space, sub-chondral sclerosis, osteophytes, and subchondral cysts (Fig 13.1);

the absence of osteoporosis, ankylosis, and erosions is istic Osteophytes tend to be largest in the plane of motion; there-fore, osteophytes at the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints are best seen on the lateral view In the hand and wrist, primary osteoarthritis typically affects the DIP and PIP joints and the basal joints of the thumb (Fig 13.2) The basal joints of the thumb are composed of the fi rst carpometacarpal (CMC) joint and the scaphoid-trapezium-trapezoid joints Isolated degenerative involvement at this specifi c site is virtually diagnos-tic of primary osteoarthritis The fi rst metatarsophalangeal (MTP) joint, hips and knees, and the cervical and lumbar spine are also common sites of involvement The metacarpophalangeal (MCP) joints, wrist, elbow, shoulder, and ankle are typically spared The severity of radiographic changes does not necessarily correlate with the severity of symptoms

character-In the knee, the characteristic distribution of involvement is

in the medial compartment and, to a less severe degree, the lofemoral compartment Joint space narrowing, subchondral sclerosis, osteophytes, and subchondral cysts are typical fi ndings (Fig 13.3) Occasionally, more severe involvement of the lateral

patel-or patellofempatel-oral compartments occurs Angular defpatel-ormities and joint space narrowing are best demonstrated on standing views

Because the severity of involvement of the anterior and rior portions of the femoral cartilage is typically uneven, the amount of joint space narrowing may vary between radiographs with the knee in extension and fl exion On MRI, early osteoar-thritis is evident as abnormal high signal in articular cartilage on T2-weighted MRI When isolated to the patella, this condition is

poste-called chondromalacia patellae (Fig 13.4) Fibrillation of the

car-tilage surface, thinning of the carcar-tilage, and frank loss of lage may be seen in progressively more severe cases Subchondral

carti-the femoral head often forms a collar of bone around carti-the femoral neck at the margin of the articular surface, usually seen best on frog lateral views As with the knee, uneven involvement of the articular cartilage results in varying amounts of joint space narrowing from position to position Mapping cartilage thickness with fl uoroscopi-cally positioned spot radiographs or cartilage-specifi c imaging parameters on MRI can be helpful in planning rotational osteoto-mies for treatment.

Osteoarthritis of the synovial joints of the spine may be the predominant feature of degenerative spine disease or may occur

in association with other features such as degenerative disk ease, previous trauma, scoliosis, kyphosis, or vertebral anomalies

dis-The common sites of synovial joint osteoarthritis are the lower cervical and lower lumbar spine The atlantoaxial joint is also synovial and may be affected The pathologic process is identical

to that of other synovial joints, leading to joint space narrowing, subchondral sclerosis, and osteophytes Loss of articular cartilage may allow subluxation or excessive motion; bony hypertrophy may reduce motion Osteophytes and ligamentous thickening may lead

to nerve root involvement These fi ndings are best demonstrated

fl uid in the joint (Fig 13.10)

Infl ammatory (erosive) osteoarthritis is a condition in which

an acute synovitis accompanies primary osteoarthritis Although joint degeneration always has some component of synovial infl ammation because of the presence of joint debris and carti-lage breakdown products, the infl ammation dominates the clini-cal presentation in erosive osteoarthritis Radiographs show the degenerative features and distribution of primary osteoarthritis,

FIGURE 13.2 Osteoarthritis at the DIP joints of the fi ngers A: PA radiograph B: Lateral radiograph.

FIGURE 13.1 Osteoarthritis at the fi rst CMC and scaphotrapezial

joints with narrowing of the articular spaces, osteophyte formation,

subchondral sclerosis, and subluxation

bone edema at sites of cartilage loss, osteophyte formation, loose

bodies, and effusions may be present in established osteoarthritis

(Figs 13.5–13.7)

In the hip, loss of articular space is usually found along the

superior (horizontal) portion of the joint (Fig 13.8) Less

com-monly, the medial joint space is narrowed Osteophyte formation in

FIGURE 13.3 Osteoarthritis with asymmetric joint space narrowing, osteophytes, and subchondral sclerosis

A: Right knee B: Left knee.

FIGURE 13.4 Chondromalacia patellae with effusion as well as

fi ssured and fi brillated patellar cartilage (arrow) shown on axial

T2-weighted, fat-saturated MRI

but the acute synovitis causes infl ammatory erosions, uniform

joint space narrowing, and sometimes ankylosis (Fig 13.11)

A characteristic “seagull” appearance may be seen on PA radiographs

at the interphalangeal (IP) joints of the fi ngers, corresponding to

central erosions and bony hypertrophy The typical age at onset

is in the fi fth or sixth decade, and women are affected far more frequently than men The infl ammation usually subsides within a few months to a couple of years, leaving the degenerative changes

In the hand, erosive osteoarthritis characteristically affects the DIP and PIP joints and the basal joints of the thumb, as does nonerosive primary osteoarthritis

Secondary Osteoarthritis

Secondary degenerative changes in the joints result from three major factors: an abnormality of the articular cartilage, loss of subchondral bony support beneath normal articular cartilage, and abnormal alignment and mechanical stress Any condition with one

of these features may lead to permanent, progressive osteoarthritis

Secondary osteoarthritis may follow infl ammatory arthritis if the infl ammatory process has caused permanent cartilage damage and

is quiescent long enough for the degenerative changes to develop

Mechanical trauma may injure the articular cartilage, which has

a limited ability for repair A fi brocartilage scar may replace aged areas of hyaline cartilage Joint debris, loose bodies, or dis-placed meniscal fragments within a joint may erode the articular cartilage Osteochondral loose bodies derive nutrition from syn-ovial fl uid and may grow Healthy cartilage wears prematurely when its underlying bony support is lost For example, collapse

dam-of the subchondral bone dam-of the femoral head after osteonecrosis leads rapidly to secondary degeneration Less obvious changes in the subchondral bone due to repetitive subclinical trauma may also lead to osteoarthritis An abnormally aligned joint or a joint that is subject to mechanical disadvantage or abnormal stresses may wear prematurely Posttraumatic osteoarthritis may follow malunion of long-bone fractures, imperfectly reduced intra-articular fractures (Fig 13.12), or posttraumatic joint instability Many forms of

FIGURE 13.5 Osteoarthritis A: Coronal T1-weighted MRI shows

cartilage loss and meniscal extrusion (arrow) in the medial

compart-ment Medial and lateral compartments are involved by osteophytes

B: Sagittal T2-weighted fat suppressed MRI shows patellofemoral

com-partment osteophytes (arrow) and cartilage loss C: Sagittal T2-weighted

fat suppressed MRI through the medial compartment shows effusion, cartilage loss, osteophytes, and degenerative posterior horn medial

meniscal tear (arrow).

FIGURE 13.6 Patellofemoral osteoarthritis Axial gradient echo MRI

shows loss of cartilage from the lateral facet of the patella and the

patel-lofemoral groove (arrows) Osteophytes are present on both sides of the

patellofemoral joint and the posterior margin of the lateral condyle An

effusion is present

FIGURE 13.7 Osteoarthritis of the knee with large, calcifi ed

intra-articular bodies in a popliteal cyst

FIGURE 13.9 Lumbar facet osteoarthritis on CT scan Osteophytes

extend into the lateral recesses bilaterally, causing nerve root compression

FIGURE 13.8 Osteoarthritis of the hip with advanced joint space

asymmetric narrowing and prominent osteophytes

FIGURE 13.10 Osteoarthritis of the acromioclavicular joint A: Axial T2-weighted fat suppressed MRI shows

subchondral edema in the clavicle and acromion (arrows) B: Oblique coronal T1-weighted MRI shows

hypertro-phy of the acromioclavicular joint (arrow) with mass effect on the supraspinatus muscle.

developmental and acquired bone and joint dysplasia lead to

early osteoarthritis, including developmental dysplasia of the hip

(Fig 13.13), Legg-Calvé-Perthes disease, and multiple epiphyseal

dysplasia The premature wear-out resulting from the abnormal

joint geometry worsens in a vicious cycle of progressive

malalign-ment, mechanical disadvantage, and abnormal stress

Femoroacetabular Impingement

Femoroacetabular impingement designates a spectrum of opmental or acquired conditions of the hip in which a morpho-logic mismatch between the femoral head and the acetabulum hip may lead to mechanical impingement of the acetabular rim on the femoral neck at the extremes of motion, restricting range of

devel-FIGURE 13.11 Infl ammatory osteoarthritis with erosions and osteophytes at the PIP joints and the fi rst CMC

joint A: Lateral radiograph B: PA radiograph.

FIGURE 13.12 Posttraumatic osteoarthritis 12 years after acetabular

fracture

FIGURE 13.13 Secondary osteoarthritis in the left

pseudoacetabu-lum (short arrow) in a 20-year-old woman with untreated DDH The native acetabulum (long arrow) is empty.

FIGURE 13.14 Femoroacetabular impingement with reactive bone changes at the femoral neck (arrows) A: AP

radiograph B: Frog lateral radiograph.

motion, causing pain, and leading to acetabular labral pathology

and degenerative changes In the cam type of

femoroacetabu-lar impingement, the morphology of the femoral head and neck

is abnormal as a result of conditions such as previous trauma,

slipped capital femoral epiphysis, or Legg-Perthes disease In the

pincer type of femoroacetabular impingement, the morphology

of the acetabulum is abnormal as a result of conditions such as acetabular retroversion or protrusio acetabuli Patients who may be anatomically predisposed to femoroacetabular impingement may

be asymptomatic if they do not engage in activities that require

FIGURE 13.15 Rotator cuff impingement A: Oblique coronal T1-weighted MRI shows osteoarthritis of the

acromioclavicular joint with hypertrophy (arrow) and mass effect on the supraspinatus muscle B: Oblique sagittal

T1-weighted MRI shows anterior hooking (arrow) of the acromion process.

FIGURE 13.16 Neuropathic osteoarthropathy Sagittal T1-weighted

MRI of the foot shows swelling, disorganization, and edema of the

is the most common lower motor neuron lesion causing pathic osteoarthropathy; other causes include alcoholism, tubercu-losis, amyloidosis, leprosy, peripheral nerve trauma, steroids, and congenital indifference to pain Syringomyelia is the most common upper motor neuron lesion; other causes include meningomyelo-cele, trauma, multiple sclerosis, tabes dorsalis (syphilis), and cord compression

neuro-Neuropathic osteoarthropathy occurs in 0.1% of all betics and in 5.0% of those with diabetic neuropathy Diabetic peripheral neuropathy causes loss of pain sensation and prop-rioception, leading to exceptional wear and tear without patient awareness of injury The most frequent site of involvement is the foot (80%), especially the tarsometatarsal, intertarsal, and MTP joints; involvement may be unilateral or bilateral Tarsal-meta-tarsal fracture dislocation (Lisfranc fracture dislocation) may occur spontaneously or with minimal trauma Extensive sclerosis, osteophytosis, fractures, bony fragmentation, subluxation, dis-location, bony debris, effusion, and subchondral cysts are com-mon fi ndings Chronic osteomyelitis is also relatively common in the diabetic foot, and the possible combination of neuropathic osteoarthropathy with infection can pose a diagnostic dilemma (Fig 13.16) MRI with gadolinium enhancement may be helpful

dia-in this circumstance

Neuropathic osteoarthropathy occurs in 25% of patients with syringomyelia The joint changes are usually in the upper extremity (80%), and they may be atrophic rather than proliferative Acute resorption of the articulating ends of the bone without evidence

of repair, gross soft-tissue swelling, and bony debris in the soft tissues are common fi ndings This process may mimic destruction from tumor or infection The most commonly involved joint is the shoulder (Fig 13.17)

extreme ranges of motion, such as ballet or yoga Radiologic

fea-tures of femoroacetabular impingement include reactive changes

in the femoral neck (Fig 13.14) and evidence of abnormal femoral

or acetabular morphology

Subacromial Impingement

Subacromial impingement syndrome of the shoulder refers to

trapping of the rotator cuff between the top of the humerus

and the undersurface of the coracoacromial arch The coracoid

process, the coracoacromial ligament, and the acromion process

form the coracoacromial arch A downward-projecting bony

excrescence or degenerative hypertrophy of the

acromioclavicu-lar joint is commonly associated with impingement syndrome

(Fig 13.15) However, impingement syndrome is considered to

be a clinical rather than a radiologic diagnosis Other

condi-tions that may impinge on the rotator cuff include congenital,

developmental, or acquired variations in the size and shape of

structures around the coracoacromial arch, including the

acro-mion and the coracoid Other types of shoulder impingement

include posterior superior glenoid impingement and

subcora-coid impingement

Neuropathic Osteoarthropathy

Neuropathic joints (Charcot joints) have lost proprioception and

deep pain sensation With continued use of the joint, relaxation

and hypotonia of the supporting structures lead to malalignment

and recurrent injury Rapidly progressive erosion of the articular

cartilage, reactive subchondral sclerosis, fractures, and

fragmenta-tion of the subchondral bone result in a disorganized joint The

presence of joint debris induces synovitis and chronic effusion

The damage and derangement may occur over a period of days

the radiologic fi ndings can be diagnostic CPPD deposition disease has been associated with hyperparathyroidism, hemochromato-sis, aging, and osteoarthritis It has been weakly associated with hypothyroidism, ochronosis, Paget disease, Wilson disease, acro-megaly, diabetes, and gout CPPD crystal deposition disease has three manifestations: chondrocalcinosis, crystal-induced synovitis, and pyrophosphate arthropathy (Table 13.2).

CPPD crystals are generated locally in the articular tissues, where asymptomatic deposits may accumulate in cartilage, joint capsules, intervertebral disks, tendons, and ligaments In cartilage, these deposits may be evident radiographically as chondrocalcino-sis Chondrocalcinosis is most common in the knees, wrists, elbows, and hips, and is found in both fi brocartilage and hyaline cartilage

Chondrocalcinosis in the menisci has high signal intensity that can mimic a meniscal tear on MRI Chondrocalcinosis in the hyaline cartilage appears as linear or punctate areas of low signal intensity, which becomes more noticeable on gradient recalled echo (GRE) sequence because of the blooming artifact

Shedding of crystals into the joint space after rupture of a deposit causes an acute, self-limited, crystal-induced synovitis

This acute synovitis is clinically similar to acute gouty arthritis and

has been known as pseudogout As with gouty arthritis, acute

epi-sodes of infl ammatory synovitis may recur intermittently During

an acute episode, CPPD crystals can be recovered by joint tion and identifi ed by polarized light microscopy or more defi nitive physical means Uncommonly, these episodes can run together into

aspira-a subaspira-acute or chronic crystaspira-al synovitis thaspira-at resembles rheumaspira-atoid arthritis, except that the large joints of the limbs tend to be involved rather than the small ones of the hands and feet

Pyrophosphate arthropathy is the degenerative result of tural joint damage caused by chronic CPPD crystal deposition and irreversible destruction of the articular cartilage The degenerative changes can be identical to osteoarthritis, but the distribution of involvement is different In the hand, the MCP joints are character-istically involved In the wrist, the radiocarpal joint is characteristi-cally involved In severe cases, the process causes gross scapholunate dissociation in association with degenerative radiocarpal changes

struc-The scaphoid and lunate separate, and the capitate migrates

proxi-mally into the resulting gap This syndrome is called scapholunate

advanced collapse, or SLAC, wrist (Figs 13.18 and 13.19) The SLAC

wrist usually includes pancompartmental degenerative ment The shoulder (glenohumeral), knee (especially patellofemo-ral), elbow, ankle, and foot (talonavicular) are the other common sites of involvement (Fig 13.20) Chondrocalcinosis need not be present, and is absent if there is no remaining cartilage Isolated severe involvement of the patellofemoral compartment of the

CRYSTAL-ASSOCIATED DISEASES

Crystal-associated joint diseases are pathologic conditions that

occur in the presence of crystals The crystals contribute to tissue

damage, but the causal relationship between crystals and tissue

damage is not well understood Crystals precipitate from the

extracellular fl uid space into the articular tissues, where they

accu-mulate Deposits of crystals may then be shed episodically into the

joint space Clearance of crystals from the joint space and articular

cartilage is poor because these structures are avascular, alymphatic,

and largely devoid of scavenger cells The presence of particles alters

the mechanical properties of the tissues, tending to make them less

elastic Articular cartilage is particularly vulnerable to damage and

ultimately undergoes degenerative changes Large crystalline

par-ticles in the joint space can cause direct abrasive damage to the

articular surfaces Small particles can cause damage by biophysical

and biochemical interactions with cell membranes and

macromole-cules and may also provoke an acute synovitis Although the precise

mechanisms mediating acute synovial infl ammation are

incom-pletely understood, different mechanisms appear to be activated

by different crystals These crystal-induced infl ammatory reactions

tend to have a sudden onset and a rapid, self-limited course The

sudden onset is probably related to the abrupt shedding of crystals

into the joint space from a deposit in the articular tissues

Crystal deposition diseases have three clinical presentations:

(a) an asymptomatic state in which crystals can be detected, (b) an

infl ammatory arthritis, and (c) a chronic destructive arthropathy

The particular diseases are defi ned by the presence of

character-istic crystals within affected joints Aspiration of the joint during

an acute infl ammatory episode may yield material in which the

associated crystal can be demonstrated The three types of crystals

that are commonly associated with joint diseases are calcium

pyro-phosphate dihydrate (CPPD), calcium hydroxyapatite, and

mono-sodium urate monohydrate (Table 13.1)

Calcium Pyrophosphate Dihydrate Crystal

Deposition Disease

CPPD crystal deposition disease is a polyarticular arthritis with

deposition of CPPD crystals in articular tissues Its initial

pre-sentation may be monoarticular The defi nitive clinical diagnosis

requires the identifi cation of CPPD crystals from joint fl uid, but

TAB LE 13.1 Crystal Deposition Diseases of Joints

Crystal Associated Clinical Conditions

CPPD Chondrocalcinosis

PseudogoutPyrophosphate arthropathyCalcium hydroxyapatite Asymptomatic calcifi cation

Calcifi c tendonitis, bursitis, and periarthritis

Calcifi c tendonitis, bursitis, and periarthritis

Chronic destructive joint diseaseMonosodium urate

monohydrate

HyperuricemiaGouty arthritisTophaceous gout

TAB LE 13.2 Clinical Syndromes of CPPD Deposition

Disease

Asymptomatic chondrocalcinosisCrystal synovitis

Acute, intermittent (pseudogout) Subacute or chronic (resembles rheumatoid arthritis)Pyrophosphate arthropathy (resembles osteoarthritis) Without attacks of pseudogout

With intermittent attacks of pseudogout Neuropathic-like (resembles neuropathic osteoarthropathy)

tissues Ion contaminants such as carbonate, magnesium, fl uoride, and chloride are present It is probably the result of multiple causes, and there may be more than one mechanism of deposition The radiologic manifestations of hydroxyapatite deposition disease are similar to other crystal-associated conditions: asymptomatic deposits, acute crystal-induced synovitis, and chronic destructive arthropathy Unlike CPPD deposition disease, hydroxyapatite depo-sition disease typically involves the tendons, ligaments, and joint capsules rather than the articular cartilage and subchondral bone.

Deposits of hydroxyapatite in the soft tissues appear on graphs as dense, homogeneous, sharply marginated, and amor-phous calcifi cations They may have linear, angular, or round shapes, and unlike chondrocalcinosis, the calcifi cations do not conform to hyaline or fi brocartilage structures Occasionally, these deposits may mimic mineralized osteoid tumor matrix, which they may resemble The soft-tissue calcifi cations of immune-mediated connective tissue diseases such as scleroderma, polymyositis, and dermatomyositis are also in the form of hydroxyapatite, but the clinical condition of hydroxyapatite deposition disease is differ-ent from these Hydroxyapatite deposition disease is thought to

radio-be a process of abnormal mineral metabolism, possibly systemic but perhaps localized only to the sites of tissue damage; the cause and pathogenesis are not understood These deposits may occur

in periarticular soft tissues as well as tendons, ligaments, capsules, entheses, and bursae (Figs 13.21–13.24) A minority of patients with hydroxyapatite deposits have symptoms Metastatic soft-tissue deposits of hydroxyapatite around joints (periarticular calcinosis, tumoral calcinosis) may be found in patients on dialysis for chronic renal failure (Fig 13.25) Because the crystals are often aqueous suspensions (milk of calcium), CT and upright radiographs may demonstrate fl uid-sediment levels The calcifi cation is diffi cult to detect on most MRI sequences, except for gradient-recalled echo sequences, because the calcifi ed collections are of low signal and isointense to the involved tendons MRI may show muscle and soft-tissue edema associated with the calcifi cations

Recurrent episodes of calcifi c tendonitis or calcifi c tis are commonly associated with hydroxyapatite deposits Most

bursi-knee or selective radiocarpal involvement of the wrist is virtually

diagnostic of pyrophosphate arthropathy Pyrophosphate

arthropa-thy is often, but not necessarily, combined with acute episodes of

crystal-induced synovitis Very severe degenerative changes may lead

to an appearance that resembles neuropathic osteoarthropathy

Hydroxyapatite Deposition Disease

Hydroxyapatite deposition disease is a heterogeneous group of

conditions that have in common the abnormal presence of

amor-phous hydroxyapatite (basic calcium phosphate) crystals in the soft

FIGURE 13.18 Pyrophosphate arthropathy with SLAC wrist

Chon-drocalcinosis involves the triangular fi brocartilage complex (arrow).

FIGURE 13.19 CPPD hand on MRI A: PA radiograph shows joint space narrowing (arrows) at the index and

middle MCP joints. B: Coronal T2-weighted MRI with fat suppression shows high signal (arrows) at the index and

middle MCP joints C: Coronal T1-weighted MRI with fat suppression following injection of gadolinium shows

enhancement (arrows) at the index and middle MCP joints.